This project represents a continuation of our major longitudinal study of a general population (The Tucson Epidemiological Study of Airways Obstructive Diseases). The sample was originally enrolled approximately 12 years ago, the ninth survey of the population has been recently completed. A very large and diverse data base has been accumulated on the greater than 1650 Tucson households containing greater than 4,000 subjects participating in the study. The major aims of this project continue to be the determination of the pathogeneses, natural histories, methods of early detection, and means of prevention of airways obstructive diseases (AOD). It is planned to complete the 15+ years of follow-up of the population which was envisioned in the initial study design within the new grant period, and to follow specific subgroups of special interest throughout the entire duration of the project. The study will continue to involve expertise from many disciplines including epidemiology, biostatistics, physiology, radiology, and clinical as well as basic immunology in order to provide a multi-disciplinary approach to the study of AOD. New analyses will emphasize the incidence of new symptoms, disease, functional impairment as well as mortality in relationship to initial characteristics of the subjects, host risk factors , exposure to provocative factors and changes in these exposures, and the course of findings early in the study. Newly developing clinically significant AOD cases will continue to be identified and studied in detail in collaboration with other SCOR projects. By determining the interactions of host and environmental factors in determinants of symptoms and physiological status over 15 years age segments beginning at birth, the data from this study will allow one to "piece together" the evolution of both persistant and reactive airways diseases from early childhood, demonstrating sequence of events finally leading to clinically significant AOD. The risk factors being studied include early childhood respiratory illnesses, evidences of atopic predisposition, signs and symptoms suggesting bronchial reactivity, protease inhibitor status, genetic background, gender and early exposure to potential bronchial irritants (such as passive smoking). Potential provocative agents which may interact including smoking, intercurrent respiratory infections, and exposure to environmental and occupational pollutants.